The human placenta has been shown to be a source of large quantities of prostanoids. Among these prostanoids, are prostaglandins (PGs), thromboxane and prostacyclin, each of which have been shown to play an important role in implantation, normal fetal development, as well as the initiation and progress of labor. However, little is known about the control of placental prostanoid production. In recent studies we have demonstrated that gonadotropin releasing hormone (GnRH), and chorionic GnRHase, a newly isolated glycoprotein of the placenta which degrades GnRH have potent prostaglandin stimulating activity. Herein, we propose to study the basal release of prostaglandins, thromboxine and prostacyclin from human term placenta in vitro. The release of these prostanoids will be determined by HPLC analysis and RIA of the medium from perifused human term placentas. Critical steps in their production will then be determined using exogenous substrate or specific enzyme inhibitors. The role of endogenous and exogenous GnRH and chorionic GnRHase on placental prostanoid release will also be studied using antiserum to or inhibitors of these factors. Also, the effect of exogenous GnRH or chorionic GnRHase in the incubation medium will be determined. In addition, the role of progesterone and estrogens in modulating placental prostanoid production as well as these steroids effect on the GnRH and chorionic GnRHase stimulation of prostaglandins, thromboxines and prostacyclin will be examined. These studies should provide us with basic infomation on placental prostanoid production and their control by GnRH chorionic GnRHase as well as defining the modulatory role of progesterone and estrogen in these hormone productions. These data may enable us to devise protocols to modify prostanoid production. Due to the very important role of prostanoids in implantation, in placental and fetal blood flow and in the initiaion and progress of labor, these studies may provide needed information which may be able to better control the outcome of abnormal pregnancies by appropriately affecting prostanoid production.